Increases in tobacco exposure biomarkers measured in non-smokers exposed to sidestream cigarette smoke under controlled conditions

The use of exposure biomarkers in measuring the impact of aqueous waste holds out promise because such tools have short response times, are of flexible use and give an indication of the type of pollution. However, their ecological significance has not yet been demonstrated. During field studies focusing on aqueous industrial waste, the correlations obtained between several biocoenotic indicators and biomarkers measured in a fresh-water bivalve (Corbicula fluminea), demonstrate the need for work to be carried out under controlled conditions. Working in partnership with the Adour Garonne Water Board, the ELF company has developed a pilot scheme incorporating such controlled conditions. This pilot is made up of 16 canals 40 m in length supplied by river water. The pilot scheme, which is currently at the validation stage, makes it possible to reconstitute an aquatic ecosystem which, once established, will be exposed to perfectly controlled pollution conditions. The responses provided by all the indicators - biocoenotic and microbiological indicators, biomarkers - will then be correlated in order to attribute an ecological significance to the biomarkers.

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The Sulfotransferase SULT1C2 Is Epigenetically Activated and Transcriptionally Induced by Tobacco Exposure and Is Associated with Patient Outcome in Lung Adenocarcinoma

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph19010416 ◽

2021 ◽

Vol 19 (1) ◽

pp. 416

Author(s):

Candace Johnson ◽

Daniel J. Mullen ◽

Suhaida A. Selamat ◽

Mihaela Campan ◽

Ite A. Offringa ◽

...

Keyword(s):

Lung Cancer ◽

Dna Methylation ◽

Lung Adenocarcinoma ◽

Binding Site ◽

Cell Line ◽

Cigarette Smoke ◽

Cell Lines ◽

Normal Lung ◽

Tobacco Exposure

Lung cancer is the leading cause of cancer-related death. Tobacco exposure is associated with 80–90% of lung cancer cases. The SULT1C2 sulfotransferase modifies xenobiotic compounds to enhance secretion but can also render these compounds carcinogenic. To determine if SULT1C2 contributes to tobacco-related carcinogenesis in the lung, we analyzed the expression and epigenetic state of SULT1C2 in human lung adenocarcinoma (LUAD) samples and in LUAD cell lines exposed to cigarette smoke condensate (CSC). SULT1C2 expression was significantly positively correlated to overall LUAD patient survival in smokers, was elevated in LUAD tumors compared to adjacent non-tumor lung, and was significantly correlated with levels of patient exposure to tobacco smoke. SULT1C2 promoter DNA methylation was inversely correlated with expression in LUAD, and hypomethylation of the SULT1C2 promoter was observed in Asian patients, as compared to Caucasians. In vitro analysis of LUAD cell lines indicates that CSC stimulates expression of SULT1C2 in a dose-dependent and cell-line-specific manner. In vitro methylation of the SULT1C2 promoter significantly decreased transcriptional activity of a reporter plasmid, and SULT1C2 expression was activated by the DNA demethylating agent 5-Aza-2′-deoxycytidine in a cell line in which the SULT1C2 promoter was hypermethylated. An aryl hydrocarbon receptor (AHR) binding site was detected spanning critical methylation sites upstream of SULT1C2. CSC exposure significantly increased AHR binding to this predicted binding site in the SULT1C2 promoter in multiple lung cell lines. Our data suggest that CSC exposure leads to activation of the AHR transcription factor, increased binding to the SULT1C2 promoter, and upregulation of SULT1C2 expression and that this process is inhibited by DNA methylation at the SULT1C2 locus. Additionally, our results suggest that the level of SULT1C2 promoter methylation and gene expression in normal lung varies depending on the race of the patient, which could in part reflect the molecular mechanisms of racial disparities seen in lung cellular responses to cigarette smoke exposure.

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Validation of biomarkers for impact evaluation of aqueous industrial waste in mesocosms

Water Science & Technology ◽

10.2166/wst.2004.0036 ◽

2004 ◽

Vol 49 (1) ◽

pp. 123-130 ◽

Cited By ~ 3

Author(s):

A. Bassères ◽

F. Simonet ◽

M. Lafont ◽

M. Coste ◽

J.-F. Narbonne

Keyword(s):

Impact Evaluation ◽

Response Times ◽

Research Programme ◽

Community Response ◽

Pilot Scheme ◽

Controlled Conditions ◽

Biomarker Response ◽

Exposure Biomarkers ◽

Pure Substances ◽

The Impact

The use of exposure biomarkers in measuring the impact of aqueous waste holds promise because such tools have short response times, are flexible in use and may give an indication about the type of pollution. However, their ecological significance has not yet been demonstrated. It is necessary to validate these responses under controlled conditions before using such biomarkers for biomonitoring. The TotalFinaElf company has developed a pilot scheme incorporating such controlled conditions. This pilot is a dynamic open mesocosm (16 channels 40 m in length supplied with river water). The research programme currently carried out in the “Pilot Rivers” aims at validating biochemical parameters (components of phases I and II (de)toxication metabolism and propionylcholinesterase activity), measured in a fresh water bivalve Corbicula fluminea as a biomarker of water quality. The comparison between biomarker responses and community ones (reference) gives information about the precocity and sensitivity of these biomarker responses. Pure substances (trichloroethylene (TCE), cadmium (CD) and anthracenic oil (AO)) have been injected during one month. Biomarker responses are as sensitive as the most sensitive community response in the presence of CD and AO. With TCE, community responses are more sensitive. Precocity of biomarker response is observed only in the presence of CD.

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E-cigarettes and Tobacco Exposure Biomarkers among American Indian Smokers

American Journal of Health Behavior ◽

10.5993/ajhb.42.6.10 ◽

2018 ◽

Vol 42 (6) ◽

pp. 101-109 ◽

Cited By ~ 5

Author(s):

Ashley L. Comiford ◽

Dorothy A. Rhoades ◽

Paul Spicer ◽

Kai Ding ◽

Justin D. Dvorak ◽

...

Keyword(s):

American Indian ◽

Tobacco Exposure ◽

Exposure Biomarkers

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Cigarette Smoke Exposure, Pediatric Lung Disease, and COVID-19

Frontiers in Physiology ◽

10.3389/fphys.2021.652198 ◽

2021 ◽

Vol 12 ◽

Author(s):

Marta Schiliro ◽

Elizabeth R. Vogel ◽

Lucia Paolini ◽

Christina M. Pabelick

Keyword(s):

Cigarette Smoking ◽

Cigarette Smoke ◽

Pediatric Population ◽

Adult Population ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Tobacco Exposure ◽

Symptomatic Infection ◽

Pediatric Populations ◽

Inflammatory Syndrome

The detrimental effects of tobacco exposure on children’s health are well known. Nonetheless, the prevalence of secondhand or direct cigarette smoke exposure (CSE) in the pediatric population has not significantly decreased over time. On the contrary, the rapid incline in use of e-cigarettes among adolescents has evoked public health concerns since increasing cases of vaping-induced acute lung injury have highlighted the potential harm of these new “smoking” devices. Two pediatric populations are especially vulnerable to the detrimental effects of cigarette smoke. The first group is former premature infants whose risk is elevated both due to their prematurity as well as other risk factors such as oxygen and mechanical ventilation to which they are disproportionately exposed. The second group is children and adolescents with chronic respiratory diseases, in particular asthma and other wheezing disorders. Coronavirus disease 2019 (COVID-19) is a spectrum of diseases caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that has spread worldwide over the last year. Here, respiratory symptoms ranging from mild to acute respiratory distress syndrome (ARDS) are at the forefront of COVID-19 cases among adults, and cigarette smoking is associated with worse outcomes in this population, and cigarette smoking is associated with worse outcomes in this population. Interestingly, SARS-CoV-2 infection affects children differently in regard to infection susceptibility, disease manifestations, and complications. Although children carry and transmit the virus, the likelihood of symptomatic infection is low, and the rates of hospitalization and death are even lower when compared to the adult population. However, multisystem inflammatory syndrome is recognized as a serious consequence of SARS-CoV-2 infection in the pediatric population. In addition, recent data demonstrate specific clinical patterns in children infected with SARS-CoV-2 who develop multisystem inflammatory syndrome vs. severe COVID-19. In this review, we highlight the pulmonary effects of CSE in vulnerable pediatric populations in the context of the ongoing SARS-CoV-2 pandemic.

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The Sulfotransferase SULT1C2 is Epigenetically Activated and Transcriptionally Induced by Tobacco Exposure and is Associated with Patient Outcome in Lung Adenocarcinoma

10.21203/rs.3.rs-795539/v1 ◽

2021 ◽

Author(s):

Candace Johnson ◽

Daniel J. Mullen ◽

Suhaida A. Selamat ◽

Mihaela Campan ◽

Ite A. Offringa ◽

...

Keyword(s):

Lung Cancer ◽

Dna Methylation ◽

Lung Adenocarcinoma ◽

Binding Site ◽

Cell Line ◽

Cigarette Smoke ◽

Cell Lines ◽

Normal Lung ◽

Tobacco Exposure

Abstract Lung cancer is the leading cause of cancer-related death. Tobacco exposure is associated with 80–90% of lung cancer cases. The SULT1C2 sulfotransferase modifies xenobiotic compounds to enhance secretion but can also render these compounds carcinogenic. To determine if SULT1C2 contributes to tobacco-related carcinogenesis in the lung, we analyzed the expression and epigenetic state of SULT1C2 in human patients in relation to smoking history as well as lung adenocarcinoma (LUAD) cell lines exposed to cigarette smoke condensate (CSC). SULT1C2 expression was significantly positively correlated to overall LUAD patient survival in smokers, was elevated in LUAD tumors, and was significantly correlated with levels of patient exposure to tobacco smoke. SULT1C2 promoter DNA methylation was inversely correlated with expression in LUAD and hypomethylation of the SULT1C2 promoter was observed in Asian patients, as compared to Caucasians. In vitro analysis of LUAD cell lines indicates that CSC stimulates expression of SULT1C2 in a dose-dependent and cell-line specific manner. In vitro methylation of the SULT1C2 promoter significantly decreased transcriptional activity or a reporter plasmid and SULT1C2 expression was activated by the DNA demethylating agent 5-Aza-2’-deoxycytidine in a cell line in which the SULT1C2 promoter was hypermethylated. An aryl hydrocarbon receptor (AHR) binding site was detected spanning critical methylation sites upstream of SULT1C2. CSC exposure significantly increased AHR binding to this predicted binding site in the SULT1C2 promoter in multiple lung cell lines. Our data suggests that CSC exposure leads to activation of the AHR transcription factor, increased binding to the SULT1C2 promoter, and upregulation of SULT1C2 expression, and that this process is inhibited by DNA methylation at the SULT1C2 locus. Additionally, our results suggest that the level of SULT1C2 promoter methylation and gene expression in normal lung varies depending on the race of the patient, which could in part reflect the molecular mechanisms of racial disparities seen in lung cellular responses to cigarette smoke exposure.

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Tidal exhaled nitric oxide in healthy, unsedated newborn infants with prenatal tobacco exposure

Journal of Applied Physiology ◽

10.1152/jappl.2002.92.1.59 ◽

2002 ◽

Vol 92 (1) ◽

pp. 59-66 ◽

Cited By ~ 42

Author(s):

Graham L. Hall ◽

Benjamin Reinmann ◽

Johannes H. Wildhaber ◽

Urs Frey

Keyword(s):

Nitric Oxide ◽

Cigarette Smoke ◽

Phase Ii ◽

Tidal Flow ◽

Newborn Infants ◽

Exhaled Nitric Oxide ◽

Outcome Parameter ◽

Tobacco Exposure ◽

Fractional Exhaled Nitric Oxide

Tidal fractional exhaled nitric oxide (Fe NO) changes were investigated in healthy, unsedated infants with or without prenatal tobacco exposure. Tidal flow (V˙), Fe NO, and CO2were measured in 20 healthy, unsedated infants [age: 25–58 days, length: 56.5 ± 2.5 (SE) cm]. NO output (V˙no) was calculated (V˙no = Fe NO × V˙). Two approaches were used to investigate within-breath changes of Fe NOand V˙no. First, we identified phases II and III from the expiratory capnogram. Second, we divided expiration into time-based quartiles. Tidal Fe NO (range: 14.5 ± 1.6 to 17.6 ± 2.1 parts/billion: quartile 4 and phase II, respectively) was not different between portions and exhibited significant negative V˙ dependence. V˙no was significantly dependent on the expiratory portion, with quartile 4 being significantly lower than the remaining expiratory portions. Infants exposed to prenatal cigarette smoke ( n = 7) exhibited significantly lower Fe NO and V˙no compared with nonexposed ( n = 13) infants. We conclude that tidal Fe NO is V˙ dependent and thatV˙no may be a more suitable outcome parameter in variable V˙ conditions. Prenatal tobacco exposure resulted in a decreased Fe NO and V˙no in infants.

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